PMID- 31488789
OWN - NLM
STAT- MEDLINE
DCOM- 20191023
LR  - 20191023
IS  - 0353-5053 (Print)
IS  - 0353-5053 (Linking)
VI  - 31
IP  - Suppl 3
DP  - 2019 Sep
TI  - Magnesium and ketamine in the treatment of depression.
PG  - 549-553
AB  - Depression affects over 121 million people annually worldwide. Relatively low 
      remission rates among depressive patients enforce the search for new therapeutic 
      solutions and an urgent need to develop faster-acting antidepressants with a 
      different mechanism of action occurs. The pathomechanism of depression postulated 
      by the monoamine hypothesis is limited. The results of abnormalities in glutamate 
      and gamma-aminobutyric acid (GABA) systems in the brains of people with mood 
      disorders allowed to develop new theories regarding pathophysiology of these 
      disorders. Glutamatergic transmission is influenced by magnesium and ketamine 
      through glutamatergic N-methyl-D-aspartate receptor (NMDAR) antagonistic effects. 
      Magnesium and ketamine have a common mechanism of action in the treatment of 
      depression: an increase in GluN2B (NMDAR subunit) expression is related to the 
      administration of both of the agents, as well as inhibition of phosphorylation of 
      eEF2 (eukaryotic elongation factor 2) in cell culture and increase of the 
      expression of BDNF in the hippocampus. Combination of ketamine and magnesium in a 
      normal magnesium level presents a superadditive effect in depression treatment. 
      Analysed substances affect the GABAergic system and have anti-inflammatory 
      effects, which is correlated with their antidepressant effect. The synergistic 
      interaction between the pharmacodynamic activity of magnesium and ketamine may be 
      of particular importance for patients with mood disorders. Further research is 
      needed to determine the relationship between magnesium levels and ketamine 
      treatment response mainly in the attempt to establish if the magnesium 
      supplementation can change ketamine treatment response time or present 
      superadditive effect.
FAU - Gorska, Natalia
AU  - Gorska N
AD  - Department of Psychiatry, Faculty of Medicine, Medical University of Gdansk, 
      Debinki St. 7 build. 25, 80-952 Gdansk, Poland, nataliagorska@gumed.edu.pl.
FAU - Slupski, Jakub
AU  - Slupski J
FAU - Szalach, Lukasz P
AU  - Szalach LP
FAU - Wlodarczyk, Adam
AU  - Wlodarczyk A
FAU - Szarmach, Joanna
AU  - Szarmach J
FAU - Jakuszkowiak-Wojten, Katarzyna
AU  - Jakuszkowiak-Wojten K
FAU - Galuszko-Wegielnik, Maria
AU  - Galuszko-Wegielnik M
FAU - Wilkowska, Alina
AU  - Wilkowska A
FAU - Wiglusz, Mariusz Stanislaw
AU  - Wiglusz MS
FAU - Cubala, Wieslaw Jerzy
AU  - Cubala WJ
LA  - eng
PT  - Journal Article
PL  - Croatia
TA  - Psychiatr Danub
JT  - Psychiatria Danubina
JID - 9424753
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Peptide Elongation Factor 2)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 690G0D6V8H (Ketamine)
RN  - I38ZP9992A (Magnesium)
SB  - IM
MH  - Antidepressive Agents/*therapeutic use
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Depression/*drug therapy
MH  - Depressive Disorder/*drug therapy
MH  - Humans
MH  - Ketamine/*therapeutic use
MH  - Magnesium/*therapeutic use
MH  - Peptide Elongation Factor 2/metabolism
MH  - Receptors, N-Methyl-D-Aspartate/metabolism
EDAT- 2019/09/07 06:00
MHDA- 2019/10/24 06:00
CRDT- 2019/09/07 06:00
PHST- 2019/09/07 06:00 [entrez]
PHST- 2019/09/07 06:00 [pubmed]
PHST- 2019/10/24 06:00 [medline]
PST - ppublish
SO  - Psychiatr Danub. 2019 Sep;31(Suppl 3):549-553.